Department of Environmental Health Sciences, School of Public Health, UAB

Scientist

Center for Aging, UAB

Research Center Scientist

Veterans Administration Medical Center, Birmingham, AL

RESEARCH INTEREST IN CUTANEOUS BIOLOGY

Dr. Katiyar has been working for the last 13 years on different aspects of cutaneous biology, such as immunology, photobiology, photocarcinogenesis and photoaging, as detailed below:

Causes, mechanism and preventive approaches of skin carcinogenesis

Dr. Katiyar's interest is to study and/or determine the causes, mechanisms and preventiom of chemical and solar ultraviolet (UV) radiation induced skin carcinogenesis (photocarcinogenesis). It is well documented that chronic exposure of solar UV radiation to human skin is primarily responsible for approximately 1.3 million new cases of squamous and basal cell carcinoma every year in the USA, thus making it the most prevalent environmental carcinogen known for humans. UV radiation is a potent producer of reactive oxygen species and can act as a tumor initiator, tumor promoter and complete carcinogen as well. Dr. Katiyar is trying to develop newer and effective chemopreventive agents, particularly dietary botanicals that can prevent the risk of UV carcinogenesis in humans. To develop newer and more effective chemopreventive agents, we use in vivo animal and human model systems and in vitro cell culture systems.

In particular, he is evaluating the chemopreventive efficacy of polyphenols isolated from green tea, milk thistle and grape seeds. Dr. Katiyar has shown that these polyphenols have anti-inflammatory and anti-oxidant properties. Because of these characteristics, polyphenols have been shown to inhibit, reverse or slow down the risk of UV-induced skin carcinogenesis. To determine the mechanism of action of these naturally occurring polyphemols or dietary botanicals, he is particularly emphasizing the anti-oxidant mechanism and modulation in immunoregulatory pathways responsible for inhibition of UV-induced adverse biological effects.

Causes, mechanism and preventive approaches of cutaneous photoaging

As in other organ systems, aging in the skin results in progressive dysfunction and diminution of the radiation reserve capacity under stress, rendering the skin more susceptible to injury and diseases. Clinical conditions associated with age-dependent dysfunction include increased ease of wounding, poor wound healing, skin cancer and infectious disease susceptibility, autoimmune reactivity to skin and drugs. The progressive susceptibility to these conditions with age is due to a combination of aging processes attributable to both chronologic (intrinsic) aging, and photoaging (extrinsic damage from the environment, mainly repeated solar light exposure). Clinically the photoaging component of skin aging accounts for the development in sun-exposed areas of wrinkling, mottled hyperpigmentation and depigmentation, coarsening of the skin, roughness, poor elastic recoil, and bruisability. These conditions adversely affect self-esteem and psychosocial well being. By contrast, intervention to reduce the stigmata of photoaging can result in improved quality of life and functionality in the elderly. Dr. Katiyar also considers that accelerated photoaging of the skin is also due to impaired oxidative defense system.

Keeping these factors under consideration, Dr. Katiyar is developing new and effective chemopreventive agents, particularly from dietary sources, which can inhibit the process of skin aging and photoaging. For this purpose, he is working on various polyphenols obtained from green tea and grape seeds and using in vitro and in vivo model systems. He determined that topical application of polyphenols from green tea on animal skin protects from UV-induced adverse biological effects associated with the photoaging of the skin.

Publications: From total more than 170 publications and 15 Book Chapters

Singh T, Prasad R and Katiyar SK: Inhibition of class I histone deacetylases in non-small cell lung cancer by honokiol leads to suppression of cancer cell growth and induction of cell death in vitro and in vivo. Epigenetics, 8:54-65, 2013.